Two conditions that can affect brain development...

Hydrocephalus

Hydrocephalus (pronunciation IPA: /ˌhaɪˌdɹoʊˈsɛfələs/) is a condition that can arise in newborns, as well as adults, resulting to swelling of the head which may lead to brain if it can not be treated.

Cerebrospinal fluid (CSF) runs through hollow caves in the nervous system which constitute the ventricular system. In hydrocephalus, it is CSF which causes swelling. CSF normally exist the ventricular system and enters the subarachnoid space where it is absorbed by blood vessels.

CSF is generated in the choroid plexus and it is when the flow from choroid plexus to subarachnoid space is impaired that the ventricles (the canals) begin to swell.

In babies the head expands to accommodate the increase in fluid. If otherwise, the fluid would compress brain tissue leading to brain damage. This is known to occur in adult victims of hydrocephalus because the adult skull can not expand, thus, compression and following brain damage occurs.

To treat hydrophalus a drainage tube is inserted into the lateral ventricle through the skull, allowing for a more regular amount of intracranial fluid.


Anencephaly and Spina bifida

Incompleteness of neural tube formation can result in this fatal condition which occurs very early on in fetal development.

During neurulation, the neural plate is folded and eventually closes. Anencephaly and Spina bifida however, are what can arise when neural tube closure does not complete itself. Depending on which end of the neural tube does not close (anterior or posterior), either condition will arise.

An anterior defect in neurulation results in anencephaly (underdevelopment of the skull and forebrain). A posterior defect will result in Spinal bifeda; a defect of the spine. Whilst anencephaly is always fatal, Spinal bifida can be survived, but only under extensive medical care.

Anencephaly and Spina bifida are believed to be caused by lack of folic acid in diet, which plays a role in DNA biosynthesis which occurs as cells divide.



Anencephaly















Spina bifida

CNS Anatomy Videos

This link will direct you to my youtube channel where I have compiled a playlist of videos instructing CNS anatomy. Anatomy can be difficult to memorize so I recommend using the videos to revise.

Benzodiazepine and GABA-gated channels

GABA-gated channels mediate inhibition in the Central Nervous System (CNS). Benzodiazephines such as Diazepam bind to the GABA(a) receptor which increases frequency of GABA-gated channel openings, allowing more Cl(-) ions through the channel at synapse, which cause negative charge hyperpolarization, promoting inhibition in the cell.
Other types of drugs, barbiturates, bind to different sites on the GABA(a) receptor and carry out different tasks which also result in IPSP responses (increasing duration of channel opening). Ethanol also binds to sites on the GABA(a) receptor.



The natural endogenous ligands (binding neurotransmitter) that should resemble benzodiazephine stuctures are yet to be found. They are assumed to exist because receptors for them exist. Similar motivation for the search of endogenous ligands arose from discovery of CB1 and CB2 receptors (cannaboid receptors) where a cannaboid-like ligand was expected to be found (and was found).

How are neurotransmitters indentified?

The first criterion by which neurotransmitters are recognized as such is that they must be stored and synthesized in the PRE-SYNAPTIC NEURON. With this in mind we turn to two methods of identifying molecules that are stored and synthesized in pre-synaptic neurons, making them worthy neurotransmitter candinates.

Immunocytochemistry is an interesting method with a number of steps. The molecule of interest (the molecule we want to determine whether or not it is neurotransmitter), is injected into the blood of an animal, causing anti-bodies to be released which bind to the 'foreign' substance. In immunology, anti-bodies are specific to chemicals they are deployed against so we can expect anti-bodies that are released to deal with (bind to) an injected substance, let's say, dopamine, to also bind to dopamine if extracted from blood and applied to brain tissue. And this is what actually occurs in the immunocytochemistry technique: the anti-bodies are extracted via withdrawing blood from the animal, and are then tracer-marked (so their activity can be located), and are then applied to brain tissue. The anti-bodies will bind to concentrations of neurotransmitter, giving us localized visual descpritions of the concentration of neurotransmitter. If a neurotransmitter and its synthesizing enzyme is found in the same axon, this helps satisfy the first criterion for idenfication as neurotransmitter.


A second method is In Situ Hybridization, another very interesting method. Here, artifical mRNA is constructed in a labatory with a specific code for binding to mRNA that synthesizes neurotransmitter synthesizing enzymes. The artifical mRNA is labelled with a radioatctive 'tag' and applied to brain tissue. The point in this method is to review locations where neurotransmitter synthesis takes place. Radioactivity of 'probe' mRNA is viewed in autoradiography where locations of synthesis will be revealed. To identify the neurotransmitter, the specific neurotransmitter that the probe mRNA sequence ultimately synthesizes will be reviewed. We have thus identified the neurotransmitter associated with the located synthesizing enzymes.



These methods of identifying neurotransmitter are currently being replaced with more up to date methods of searching for neurotransmitter via receptors.